Cambridge - my notes Flashcards
(324 cards)
1
Q
Atherosclerosis
A
Atheromas (fatty deposits) and sclerosis (hardening or stiffening of the blood vessel walls).
2
Q
What causes atherosclerosis?
A
Chronic inflammation and activation of the immune system (in the artery wall) deposition of lipids in the wall atheromatous plaques
3
Q
What do atheromatous plaques result in?
A
Stiffening (HTN)Stenosis (reduced blood flow)Plaque rupture (thrombus)
4
Q
CVD modifiable risk factors
A
- Raised cholesterol* Smoking* Alcohol consumption* Poor diet* Lack of exercise* Obesity* Poor sleep* Stress
5
Q
CVD non-modifiable risk factors
A
- Older age* Family history* Male
6
Q
Co-morbidities increasing risk of atherosclerosis
A
- DM- HTN- CKD- RA- Atypical antipsychotic medications
7
Q
End results of atherosclerosis
A
- Angina- MI- TIA- Stroke- Peripheral arterial disease- Chronic mesenteric ischaemia
8
Q
NICE guidelines physical activity recommendations
A
- Aerobic activity 150min moderate intensity or 75min vigorous intensity- Strength training 2x week
9
Q
QRISK 3
A
% risk of having a stroke or MI in the next 10years
10
Q
QRISK 3 >10% treatment
A
Atorvastatin 20mg at night
11
Q
What pts get atorvastatin 20mg as 1* prevention?
A
CKD T1DM >40yo, or for 10y
12
Q
Statins mode of action
A
Reduce cholesterol production in the liver by inhibiting HMG CoA reductase
13
Q
Side effects of Statins
A
- Myopathy
- Rhabdomyolysis
- T2DM
- Haemorrhagic strokes
14
Q
Blood tests in pts on statins
A
LFTs at 3 months and 12 months (statins cause ALT and AST rise)
15
Q
How to check for rhabdomyolysis?
A
Check creatinine kinease levels
16
Q
2 examples of cholesterol lowering drugs
A
Ezetimibe (reduces cholesterol absorption in intestine)Monoclonal antibodies
17
Q
2* prevention CVD
A
- Antiplatelet medications (aspirin/clopidogrel/ticagrelor)
- Atorvastatin 80mg
- Atenolol (or Bisoprolol, Beta blocker)
- ACE inhibitor (ramipril)
18
Q
Medications post MI
A
Dual antiplatelet treatment - Aspirin 75mg daily forever- Clopidogrel or ticagrelor for 12mth
19
Q
When is Clopidogrel a preferred antiplatelet?
A
Peripheral arterial disease, and following ischaemic stroke
20
Q
Familial hypercholesterolaemia
A
AD- Family history of CVD- Very high cholesterol 7.5mmol/L- Tendon xanthomata
21
Q
Define tendon xanthomata
A
Hard nodules in tendons, containing cholesterol
22
Q
Mx of familial hypercholesterolaemia
A
- Genetic testing, specialist referral- Statins
23
Q
What causes angina?
A
Atherosclerosis affecting coronary arteries, and reducing blood flow to the myocardium
24
Q
Symptoms of angina
A
Constricting chest pain, with or without radiation to jaw and arms
25
Define stable angina
Symptoms only come with exertion, and are relieved by rest or GTN
26
Define unstable angina
Symptoms appear randomly at rest. (Type of Acute coronary syndrome)
27
Define cardiac stress testing
Assessing heart function in exertion – treadmill or dobutamine – assess by ECG, Echo, MRI
28
Gold standard Ix for coronary artery disease
Invasive coronary angiography
29
Immediate symptomatic relief in angina
Sublingual GTN
30
What is the effect of GTN (and what side effects?)
Vasodilation (headache, dizziness)
31
How to use GTN
1st take GTN, after 5 min 2nd dose if symptoms, again after 5 min 3rd dose, after 5min call ambulance
32
Long term symptomatic relief in angina
Beta blocker (bisoprolol) AND/OR Ca Channel blocker (diltiazem/verapamil)
33
When should diltiazem and verapamil be avoided?
In heart failure with reduced ejection fraction
34
Surgical interventions in Angina
- PCI (coronary angioplasty and stenting)
- CABG
35
3 options for graft in CABG
- Saphenous vein- Internal thoracic artery- Radial artery
36
Acute Coronary Syndrome
Result of a thrombus from atherosclerotic plaque, blocking a coronary artery
37
3 types of ACS
- Unstable angina- STEMI- NSTEMI
38
Right coronary artery supplies (areas)
R atrium
R ventricle
Inferior L ventricle
Posterior septum
39
Left coronary artery branches
Circumflex artery, Left anterior descending
40
Circumflex artery supplies (areas)
L atrium
Posterior L ventricle
41
Left anterior descending supplies (areas)
Anterior aspect of L ventricle
Anterior aspect of septum
42
What pts are at risk of silent MI?
Diabetic pts
43
STEMI ECG changes
ST elevationLBBB
44
NSTEMI ECG changes
ST depressionT wave inversion
45
Pathological Q waves significance
Transmural infarction (involving full muscle thickness)
Appear 6h post symptoms onset
46
Left coronary artery (heart area, ECG leads)
Anterolateral, I, aVL, V3-6
47
Left anterior descending area and leads
Anterior, V1-4
48
Circumflex a (area and leads)
Lateral, I, aVL, V5-6
49
Right coronary artery area and leads
Inferior, II, III, aVF
50
Rise of troponin significance
MI
51
Ix in suspected ACS
Troponin (rising or high)BloodsChest x ray Echocardiogram
52
STEMI Dx
ECG: - ST elevation- LBBB
53
NSTEMI Dx
Raised troponin + Normal ECG OR ST depression OR T wave inversion
54
Unstable angina Dx
Symptoms of ACS + normal troponin + normal ECG OR ST depression OR T wave inversion
55
Acute coronary syndrome initial Mx
C- call ambulanceP – perform ECGA – aspirin 300mgI – IV morphine with antiemetic (metoclopramide)N – nitrate (GTN)
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Pt pain free, pain in the last 72h Mx
Refer for same-day assessment
57
Pt with STEMI within 12h of onset Mx
PCI <2h of presenting OR Thrombolysis <2h of presenting
58
Define thrombolysis
Injecting a fibrinolytic agent (breaks down clots)
59
Example of thrombolytics
Streptokinase, alteplase, tenecteplase
60
NSTEMI Mx
B – Angiography or PCIA – Aspirin 300mgT – Ticagrelor 180mg statM – morphine A – antithrombin (fondaparinux) N – GTN O2 if saturation drops <95%
61
Angiography in NSTEMI
Immediate angiography in unstable patients
62
GRACE score
6-months probability of death after NSTEMI
63
=< 3% GRACE score
Low risk
64
>= 3% GRAE score
Medium – High risk
65
Pericarditis
Inflammation of the pericardium
66
2 Most common causes of pericarditis
Idiopathic or viralOther: autoimmune, injury, cancer, uraemia, methotrexate
67
Pericarditis presentation
Chest pain, fever
68
Tx of pericarditis
NSAIDs
69
Define pericardial effusion
Potential space of the pericardial cavity fills with fluids; makes it difficult to expand during diastole
70
Pericardial/cardiac tamponade
Pericardial effusion is large enough to raise intra-pericardial pressure (reduced heart filling in diastole, decreases Cardiac Output in systole)
71
Describe the character of chest pain in pericarditis
Sharp, central, pleuritic – worse with inspiration, worse on lying down, better on sitting forward
72
Auscultation sign in pericarditis
Pericardial rub
73
Pericardial Ix (blood tests)
Raised white cells, CRP, ESR
74
Pericardial Ix ECG changes
Saddle-shaped ST elevation; PR depression
75
Mx of pericarditis
NSTEMI, colchicine (3 months to reduce recurrence risk)
76
Pericardiocentesis
Removal of fluid from around the heart in significant pericardial effusion/tamponade
77
Acute left ventricular failure
Left ventricular unable to move blood through left side of heart info the systemic circulation
78
Cardiac output
Volume of blood ejected by heart per minute
79
Stroke volume
Volume of blood ejected during each beat
80
Volume of blood ejected during each beat
Stroke volume x heart rate
81
Pulmonary oedema
Lung tissue and alveoli are filled with interstitial fluid; interferes with gas exchange and causes SOB and reduced O2 sats
82
Presentation of acute left ventricular failure
- Acute SOB - Exacerbated by lying flat- Better by sitting up
83
What kind of respiratory failure is acute left ventricular failure?
Type 1 respiratory failure (low oxygen without increased carbon dioxide)
84
Symptoms of acute left ventricular failure
SOBLooking unwellCough with frothy white or pink sputum
85
Signs in acute left ventricular failure
Raised RRReduced SaO2Tachycardia3rd heart soundBilateral basal crackles (wet sound)Hypotension
86
Right sided heart failure symptoms
Peripheral oedema (legs ankles sacrum)Raised JVP (due to backlog of blood in right heart)
87
B-type Natriuretic Peptide
BNP/ hormone released from the heart ventricles when myocardium is too stretched (suggest heart overload)
88
Action of BNP on cardiac system
Relax smooth muscle in blood vessels, reduces systemic vascular resistance
89
Action of BNP on kidneys
Acts as a diuretic to promote water excretion
90
Ejection fraction
Measure of left ventricular function (% of blood pumped out of the ventricle with each contraction) >50%
91
Cardiomegaly
Cardiothoracic ratio >0.5
92
Lung oedema (fluid leaking) X ray signs
Bilateral pleural effusionsInterlobar fissure fluidFluid in septal lines (Kerley lines)
93
Mx of pleural effusion
Sit upO2Diuretics (IV furosemide)IV fluids STOPPED
94
Positive inotropes
Increase the contractility of the heart increase CO and MAP
95
Vasopressors
Cause vasoconstriction, increase systemic vascular resistance and MAP
96
Heart failure with reduced ejection fraction
Ejection fraction <50%
97
Heart failure with preserved ejection fraction
>50%; diastolic dysfunction
98
Causes of chronic heart failure
* Ischaemic heart disease* Valvular heart disease (aortic stenosis)* Hypertension* Arrhythmias (AF)* Cardiomyopathy
99
Symptoms of chronic heart failure
* Breathlessness, worsened by exertion* Cough (frothy white/pink sputum)* Orthopnoea* Paroxysmal nocturnal dyspnoea* Peripheral oedema* Fatigue
100
Signs of examination in chronic heart failure
* Tachycardia* Tachypnoea * HTN* 3rd heart sound * Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema* Raised jugular venous pressure (JVP* Peripheral oedema
101
Orthopnoea
Breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
102
Paroxysmal Nocturnal Dyspnoea
suddenly waking at night with a severe attack of shortness of breath, cough and wheeze
103
Dx of heart failure
ECGEchocardiogramNT-proBNP
104
New York Heart Association (NYHA)
Grades severity of symptoms related to heart failure
105
Classes of NYHA
* Class I: No limitation on activity* Class II: Comfortable at rest but symptomatic with ordinary activities* Class III: Comfortable at rest but symptomatic with any activity* Class IV: Symptomatic at rest
106
Mx if NT-proBNP 400-2000 ng/litre
Seen and Echo within 6 weeks
107
Mx if NT-proBNP >2000 ng/litre
Seen and Echo within 2 weeks
108
Tx of chronic heart failure
Ace inhibitor (ramipril)Beta blocker (bisoprolol)Aldosterone antagonist (when symptoms not controlled with A and B – spironolactone or eplerenoneLoop diuretics (furosemide or bumetanide)
109
Which drugs must be avoided in valvular heart disease?
ACE inhibitors
110
When are aldosterone antagonists used in reduced EF?
When symptoms are not controlled on ACEi + B Blocker
111
Who needs a implantable cardioverter defibrillators?
Pts with shockable arrythmia such as ventricular tachycardia OR ventricular fibrillation
112
Cardiac resynchronisation therapy
Used in EF <35%Biventricular (Triple chamber)pacemaker – RA, RV, LV
113
Hypertension (levels)
>140/90 clinical setting; >135/85 home/ambulatory
114
Essential hypertension
~primary hypertension / no secondary cause
115
2* hypertension causes
Renal diseaseObesityPregnancy/Pre-eclampsiaEndocrineDrugs (alcohol, nsaids, oestrogen, liquorice)
116
Most common cause of 2* HTN
Renal disease (renal artery stenosis)
117
How is renal artery stenosis diagnosed?
Duplex ultrasound or MR/CT angio
118
If HTN <40 yo
Specialist investigations
119
Endocrine cause of HTN
Hyperaldosteronism (Conn’s syndrome)
120
BP >140/90 steps
24h ambulatory BP or home readings
121
White coat effect
>20/10 difference in BP between clinic and home
122
HTN stage 1
Clinic >140/90; Home 135/85
123
HTN Stage 2
Clinic >160/100; Home 150/95
124
HTN Stage 3
>180/120
125
What to test in pts with new HTN diagnosis?
- HbA1c, renal function, lipids- Urine Albumin:Creatinine- Proteinura and dipstick for haematuria- ECG for left ventricular hypertrophy - Eye exam
126
QRISK
Risk of stroke or MI in next 10 years
127
QRISK >10%
Take atorvastatin 20mg at night
128
What are the steps of HTN medications in Black African / Black Caribbean people?
ARB – instead of ACEi (candesartan)B blocker (bisoprolol)Ca channel blocker (amlodipine)Diuretic (thiazide like) (indapamide)
129
Which HTN drugs are not used together?
ARB and ACEi
130
What drug is given if pt doesn’t tolerate Calcium channel blockers?
Thiazide-like diuretic
131
SE of calcium channel blockers (amlodipine)
Ankle oedema
132
HTN drugs steps in <55 or any age diabetes
1: ACEi or ARB2: A + C or A + D3: A + C + D4. K+ <4.5 then low dose spironolactoneK+ >4.5 then alpha or beta blocker
133
HTN drugs steps in >=55 (no diabetes) or black
1: C2: C + A or C + D3: A + C + D4. K+ <4.5 then low dose spironolactoneK+ >4.5 then alpha (Doxazosin) or beta blocker (atenolol)
134
Mode of action of aldosterone
Blocks action of aldosterone in the kidneys (sodium excretion, potassium reabsorption)
135
SE of thiazide diuretics
Cause hypokalaemia
136
SE of spironolactone or ACE i
hyperkalaemia
137
<80 yo BP target
<140 / <90
138
>80 yo BP target
<150 / <90
139
Malignant hypertension
BP > 180/120, retinal haemorrhages or papilloedema
140
Hypertensive emergency drugs
* Sodium nitroprusside * Labetalol* Glyceryl trinitrate* Nicardipine
141
first heart sound (S1)
closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.
142
second heart sound (S2)
closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete.
143
third heart sound (S3)
0.1 sec after S2 – gallop rhythm – due to pulling the chordae tendineae
144
What does gallop rhythm / S3 indicate in elderly?
Heart failure- S3 normal in 15-40yo
145
fourth heart sound (S4)
Heard directly before S1 – ALWAYS abnormal
146
What does S4 indicate?
Stiff or hypertrophic ventricle
147
Where is Erb’s point?
3rd intercostal space, left sternal border – best to hear S1 and S2
148
How to hear mitral stenosis better?
Pt lying on left side
149
How to hear aortic regurgitation better?
Pt sat up, leaning forward, holding exhalation
150
Which murmur is heard over carotids?
Aortic stenosis
151
Which murmur is heart in the left axilla?
Mitral regurgitation
152
Which valvular disease causes hypertrophy?
Stenosis (mitral or aortic)
153
What does mitral stenosis cause?
Left atrial hypertrophy
154
What does aortic stenosis cause?
Left ventricular hypertrophy
155
What valvular disease causes dilatation?
Regurgitation (mitral or aortic)
156
What does mitral regurgitation cause?
Left atrial dilatation
157
What does aortic regurgitation cause?
Left ventricular dilatation
158
Most common valvular heart disease?
Aortic stenosis
159
Most common indication for valve replacement?
Aortic stenosis
160
Aortic stenosis
Narrowing of the aortic valve – restricting blood flow from left ventricle to aorta
161
Aortic stenosis murmur characteristics
Ejection – systolic High-pitched Crescendo-decrescendo Radiates to carotidsNarrow pulse pressureSlow rising pulseExertional syncope
162
Causes of aortic stenosis
Idiopathic age-related calcification Bicuspid aortic valve Rheumatic heart disease
163
Aortic regurgitation
Incompetent aortic valve – blood flows back from the aorta to the left ventricle
164
Aortic regurgitation murmur characteristics
Early diastolic Soft murmur Collapsing pulseWide pulse pressure Heart failure and pulmonary oedema Also: Austin-Flint murmur – heard at apex
165
Collapsing pulse
In aortic regurgitation Also called water hammer pulse – appearing and rapidly disappearing pulse – felt in the radial artery (when arm held straight upward)
166
Causes of aortic regurgitation
* Idiopathic age-related weakness* Bicuspid aortic valve* Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
167
Narrowed mitral valve, restricting blood flow from the left atrium to the left ventricle
Narrowed mitral valve, restricting blood flow from the left atrium to the left ventricle
168
Mitral stenosis murmur
Mid diastolic Low pitched (rumbling) Loud S1 (tapping apex beat)AF – irregularly irregular pulseMalar flush
169
Malar flush
Present in mitral stenosis; red discolouration of the skin of cheeks and nose; due to back pressure of pulmonary system causing a rise in CO2 and vasodilation
170
Causes of mitral stenosis
* Rheumatic heart disease* Infective endocarditis
171
Mitral regurgitation
Incompetent mitral valve – blood flows back from left ventricle to the left atrium during systolic contraction (causes reduced ejection fraction and congestive cardiac failure)
172
2nd most common cause of valve replacement
Mitral regurgitation (1st is aortic stenosis)
173
Mitral regurgitation murmur
Pan-systolic High-pitched (whistling)Radiates to left axilla 3rd heart soundThrill AF – irregularly irregular pulseHeart failure and pulmonary oedema
174
Causes of mitral regurgitation
* Idiopathic * Ischaemic heart disease* Infective endocarditis* Rheumatic heart disease* Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome
175
Tricuspid regurgitation
Incompetent tricuspid valve – blood flows back from right ventricle to the right atrium during systolic contraction
176
Tricuspid regurgitation murmur
Pan-systolic Split 2nd heart sound (pulmonary valve closes faster than aortic valve/ left ventricle empties faster than right)Raised JVP Giant C-V waves (Lancisi’s sign)Pulsatile liverPeripheral oedemaascites
177
Causes of tricuspid regurgitation
* Infective endocarditis* Rheumatic heart disease* Carcinoid syndrome* Ebstein’s anomaly* Connective tissue disorders, such as Marfan syndrome
178
Pulmonary stenosis
Narrowed pulmonary valve – restricts blood flow from right ventricle to pulmonary arteries
179
Pulmonary stenosis murmur
Ejection systolic (louder with inspiration)Split 2nd heart sound (left ventricle empties faster than the right)Raised JVPGiant A waves (right atrium contracts against right hypertrophic ventricle) Peripheral oedema ascites
180
Pulmonary stenosis causes
Congenital: - Noonan syndrome- Tetralogy of fallot
181
Tetralogy of fallot
* Ventricular septal defect (VSD)* Overriding aorta* Pulmonary valve stenosis* Right ventricular hypertrophy
182
Bioprosthetic valve
Limited life span (10 years)Porcine valves – come from pigs
183
Mechanical valves
20 y life span Lifelong anticoagulation with warfarin INR target 2.5-3.5
184
AF INR target
2-3
185
Metallic mitral valves click
Replaces S1
186
Types of valves
Starr Edwards (with ball in a cage) – not used due to thrombus formationTilting disc valve – single tilting discSt Jude valves – bileaflet valves – smallest risk of thrombus
187
Metallic aortic valves click
Replaces S2
188
Mechanical heart valves complications
* Thrombus formation (blood stagnates and clots)* Infective endocarditis (infection in the prosthesis)* Haemolysis causing anaemia (blood gets churned up in the valve)
189
TAVI
Transcatheter aortic valve implantation – treatment for severe aortic stenosis – catheter inserted into femoral artery, implanting a bioprosthetic valve
190
Infective endocarditis mortality rate
15%
191
Infective endocarditis causative organisms
Gram-positive cocci* Staphylococcus* Streptococcus* Enterococcus
192
Infective endocarditis
Infection of the endothelium (inner heart surface) – affects heart valves and can be acute/subacute/chronic
193
Risk factors for infective endocarditis
* Intravenous drug use* Structural heart pathology * Chronic kidney disease * Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)* History of infective endocarditis
194
Structural pathologies increasing risk of endocarditis
* Valvular heart disease* Congenital heart disease* Hypertrophic cardiomyopathy* Prosthetic heart valves* Implantable cardiac devices (e.g.,pacemakers)
195
Causes of infective endocarditis
* Staphylococcus aureus. * Streptococcus (viridans)* Enterococcus (e.g., Enterococcus faecalis)
196
Symptoms of infective endocarditis
Fever Night sweatsMuscle acheLoss of appetite
197
Examination findings in infective endocarditis
* New or “changing” heart murmur* Splinter haemorrhages * Petechiae * Janeway lesions* Osler’s nodes * Roth spots (haemorrhages on the retina)* Splenomegaly * Finger clubbing
198
Petechiae
(small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
199
Osler’s nodes
(tender red/purple nodules on the pads of the fingers and toes)
200
Janeway lesions
(painless red flat macules on the palms of the hands and soles of the feet)
201
Blood tests for infective endocarditis
Blood cultures – 3 cultures separated by 6h from 3 different sites
202
Imaging in infective endocarditis
Echocardiography, transoesophageal echocardiography, For prosthetic valves: PET/CT or SPECT/CT
203
Modified Duke criteria
Diagnosis of infective endocarditis (1 major + 3 minor OR 5 minor)
204
Duke criteria (major and minor)
Major: +ve blood cultures, imaging findings Minor: predisposition, fever, vascular phenomena, immunological phenomena, microbiological phenomena
205
Mx of infective endocarditis
IV broad spectrum abx (amoxicillin and optional gentamycin) - 4 weeks for native valves- 6 weeks for prosthetic valves
206
When is surgery required in infective endocarditis?
- Heart failure relating to valve pathology- Large vegetations - Infections not responding to abx
207
Hypertrophic obstructive cardiomyopathy (HOCM)
Left ventricle becomes hypertrophic Autosomal Dominant (defect in gene of sarcomere proteins)
208
left ventricular outflow tract obstruction
Hypertrophic obstructive cardiomyopathy asymmetrically affects the septum, blocking the outflow of blood from the left ventricle
209
HOCM examination findings
Ejection systolic murmur (lower left sternal vorder)4th heart sound Trhill (lower left sternal border)
210
What medications are avoided in HCOM?
ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.
211
Ix in HOCM
Echocardiogram or cardiac MRI Genetic testingChest x ray (normal/pulmonary oedema)ECG (left ventricular hypertrophy)
212
Mx of HOCM
* Beta blockers* Surgical myectomy * Alcohol septal* Implantable cardioverter defibrillator * Heart transplant
213
Dilated cardiomyopathy
heart muscle becomes thin and dilated
214
Alcohol-induced cardiomyopathy
dilated cardiomyopathy caused by long-term alcohol use.
215
Restrictive cardiomyopathy
heart becomes rigid and stiff, causing impaired ventricular filling during diastole.
216
Arrhythmogenic cardiomyopathy
Genetic condition Heart muscle is replaced with fibrofatty tissue ->Cause of sudden cardiac death in athletes
217
Takotsubo cardiomyopathy
Left ventricular dysfunction and weakness Follows emotional stress – Broken heart syndrome
218
Symptoms of AF
SOBDizziness Syncope Stroke Palpitations Irregularly irregular choice
219
AF
Electrical activity in the atria becomes disorganised; fibrillation – random muscle twitching- Irregularly irregular ventricular contractions - Tachycardia- Heart failure - Increased stroke risk
220
2 differential diagnoses for irregularly irregular pulse:
AFVentricular ectopics (Disappear at high heart rate)
221
Causes of AF
SepsisMitral valve pathology (stenosis or regurgitation)Ischaemic heart diseaseThyrotoxicosisHypertensionAlcohol and caffeine
222
ECG in AF
Absent P wavesNarrow QRS tachycardiaIrregularly irregular ventricular rhythm
223
Paroxysmal atrial fibrillation
episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. they last between 30sec - 48 hours.
224
Ix for Paroxysmal atrial fibrillation
* 24-hour ambulatory ECG (Holter monitor)* Cardiac event recorder lasting 1-2 weeks
225
Valvular Atrial Fibrillation
AF with significant mitral stenosis or a mechanical heart valve. (AF without valve pathology is non-valvular AF)
226
AF treatment
* Rate or rhythm control* Anticoagulation to prevent strokes
227
Rate control
1st step for pts with AF (except reversible cause of AF, onset within 48h, heart failure)Aim for Heart rate <100
228
Rate control drugs
B blocker (1st line) – atenolol, bisoprololCa channel blocker (diltiazem or veramapil) – DO NOT give in heart failureDigoxin – only in sedentary people, toxic, needs close monitoring
229
Rhythm control
Aims to restore normal sinus rhythm Offered to pts with:- Reversible cause AF- New onset AF within 48h- Heart failure caused by atrial fibrillation
230
Rhythm control process
Either - Cardioversion (immediate or delayed)- Long-term rhythm control
231
Immediate cardioversion
* AF for less than 48 hours * Causing life-threatening haemodynamic instability* Either electrical or pharmacological
232
Immediate pharmacological cardioversion
* Flecainide* Amiodarone
233
Drug of choice in AF cardioversion in structural heart disease?
amiodarone
234
Electrical cardioversion
Shock the heart back into sinus rhythm (cardiac defibilator, sedation or general anaesthesia)cardioversion
235
Delayed cardioversion
Used in AF >48h - Electrical - Transoesophageal echocardiography-guided cardioversion - Amiodarone added before and after electrical cardioversion to prevent recurrence
236
Anticoagulation in delayed cardioversion
For at least 3 weeks before cardioversion Pts are rate controlled in the meantime
237
Long term rhythm control drugs
* Beta blockers 1st* Dronedarone 2nd* Amiodarone is useful in patients with heart failure or left ventricular dysfunction
238
Mx of paroxysmal AF
Pill-in-the-pocket For pts with infrequent episodes and no structural heart disease Take a pill when symptoms starting
239
Paroxysmal AF drugs
Flecainide – pill in the pocket – might convert AF into atrial flutter with 1:1 AV conduction
240
When is ablation needed?
When rate or rhythm control drug treatment is inadequate
241
Atrioventricular node ablation
Destroys the av node; permanent pacemaker is required to control ventricular contraction
242
Anticoagulation in AF
DOAC 1st line Warfarin
243
Left atrial ablation
Performed in cath lab under sedation/GA – catheter inserted into femoral vein to the left atrium- radiofrequency ablation (heat) burns the abnormal electrical activity areas
244
Risk of stroke in AF
Without anticoagulation: 5%With 1-2% per year
245
DOAC
Do not require INR monitoring 6-14h half life
246
Direct thrombin inhibitor
Dabigatran
247
Direct Xa factor inhibitors
Apixaban, edoxaban and rivaroxaban
248
Which DOACs are taken 1x daily
edoxaban and rivaroxaban
249
Which DOACs are taken 2x daily
Apixaban and dabigatran
250
How to reverse apixaban and rivaroxaban action?
Andexanet alfa
251
How to reverse dabigatran action?
Idarucizumab
252
Indications for DOACs
* Stroke prevention in patients with AF* Treatment of (DVT) and (PE)* Prophylaxis of venous thromboembolism (DVTs and PEs) after a hip or knee replacement
253
Advantages of DOACs over warfarin
No monitoring required No major interactionsLess bleeding risk than warfarinBetter control of strokes in AF than warfarin
254
Warfarin
Vit K antagonist – prolongs prothrombin time (time taken for blood to clot)
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INR
Assesses how coagulated pt is INR 1 – normal prothrombin time INR 2 – prothrombin time twice as normal
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Target INR for AF
2-3
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TTR time in therapeutic range
Refers to percentage of time that INR is in the target range (when INR is too low, risk of stroke, when too high, risk of bleeding)
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CHA2DS2-VASc
Assess whether patient with AF should start anticoagulation. The higher the score, the higher risk of stroke or TIA
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How to reverse vit K effects?
Vit K
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CHA2DS2-VASc of 2
Offer anticoagulation
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CHA2DS2-VASc score
* C – Congestive heart failure* H – Hypertension* A2 – Age above 75 (scores 2)* D – Diabetes* S2 – Stroke or TIA previously (scores 2)* V – Vascular disease* A – Age 65 – 74* S – Sex (female)
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ORBIT score
Assesses risk of major bleeding in pts with AF taking anticoagulation
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CHA2DS2-VASc of 1
Consider anticoagulation in men (women automatically score of 1)
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CHA2DS2-VASc of 0
No anticoagulation
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ORBIT score factors
* O – Older age (age 75 or above)* R – Renal impairment (GFR <60)* B – Bleeding previously (history of gastrointestinal or intracranial bleeding)* I – Iron (low haemoglobin or haematocrit)* T – Taking antiplatelet medication
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Left atrial appendage occlusion
Used in pts with contraindications for anticoagulation and high stroke risk Plug is placed in left atrial appendage preventing blood pooling/accessing the area
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Supraventricular tachycardia
Caused by electrical signal re-entering the atria from the ventricles; the signal travels through atrioventricular node again -> narrow complex tachycardia (QRS has a duration of <0.12 seconds)
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AF on ECG
* Absent P waves* Narrow QRS complex tachycardia* Irregularly irregular ventricular rhythm
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Atrial flutter on ECG
Atrial rate is 300 beats Saw-tooth pattern 2 atrial contractions per 1 ventricular contraction
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Sinus tachycardia on ECG
Normal P wave, QRS, T wave
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3 types of SVT
- Atrioventricular nodal re-entrant tachycardia- Atrioventricular re-entrant tachycardia- Atrial tachycardia
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Supraventricular tachycardia on ECG
QRS followed immediately by T wave P waves are present by buried in the T waves Different from AF – regular rhythm Different from atrial flutter – no saw-tooth patternNarrow complex tachycardia Occurs at rest with no cause (sinus tachy has gradual onset and explanation – pain/fever)
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Atrioventricular re-entrant tachycardia
Re-entry point is an accessory pathway (somewhere between atria and ventricles)- This is called Wolff-Parkinson-White syndrome
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What is a Delta wave on ECG
Slurred upstroke on QRS complex
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Atrioventricular nodal re-entrant tachycardia
The re-entry point is via atrioventricular node (most common type of SVT)
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Atrial tachycardia
Electrical signal originates in the atria but outside the sinoatrial node (abnormally generated electrical activity)
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Treatment for WPW syndrome
Radiofrequency ablation of the accessory pathway
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Wolff-Parkinson-White syndrome
Extra electrical pathway connecting the atria and ventricles (also called pre-excitation syndrome)Extra pathway is called Bundle of Kent
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Wolff-Parkinson-White on ECG
* Short PR interval, less than 0.12 seconds* Wide QRS complex, greater than 0.12 seconds* Delta wave
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Valsalva manoeuvres
Increase thoracic pressure (pt blows against resistance for 10-15sec)
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vagal manouvres
Stimulate the vagus nerve, increase the activity of parasympathetic nervous system (slow conduction of electrical activity in the heart)
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What drugs are contraindicated in WPW?
Anti-arrhythmic (beta blockers, calcium channel blockers, digoxin, adenosine) – as they promote conduction through the accessory pathway and lead to wide complex tachycardia
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WPW treatment
Step 1: Vagal manoeuvresStep 2: AdenosineStep 3: Verapamil or a beta blockerStep 4: Synchronised DC cardioversion (IV amiodarone added if DC unsuccessful)
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How to give adenosine?
Rapid IV bolus, grey cannula* Initially 6mg* Then 12mg (after 2 mins)* Then 18mg
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Carotid sinus massage
Stimulating baroreceptors
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adenosine
Slows cardiac conduction through AV node (might inially cause asystole or bradycardia)
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When is Synchronised DC applied?
During R wave (ventricular contraction) Avoid T wave – will cause ventricular fibrillation
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What arrhythmias can be resolved by radiofrequency ablation?
* Atrial fibrillation* Atrial flutter* Supraventricular tachycardias * Wolff-Parkinson-White syndrome
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Mx of paroxysmal SVT
- Long term (b blockers, ca channel blockers, amiodarone)- Radiofrequency ablation
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Diving reflex
Submerging pt’s face in cold water
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Which pts shouldn’t take adenosine?
* Asthma* COPD* Heart failure* Heart block* Severe hypotension * Potential atrial arrhythmia with underlying pre-excitation
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Shockable pulseless rhythms
* Ventricular tachycardia* Ventricular fibrillation
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non shockable pulseless rhythm
* Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)* Asystole (no significant electrical activity)
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Narrow complex tachycardia (4 differentials)
QRS complex <0.12 sec (3 small squares)- Sinus tachycardia- Supraventricular tachycardia (vagal manouvres and adenosine)- Atrial fibrillation (rate control or rhythm control)- Atrial flutter (rate control or rhythm control)
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Broad complex tachycardia (4 differentials)
QRS >0.12 sec (3 small squares)- Ventricular tachycardia (treated with IV amiodarone)- Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)- Atrial fibrillation with bundle branch block (treated as AF)- Supraventricular tachycardia with bundle branch block (treated as SVT)
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Life threatening arrythmia features – treatment
Synchronised DC cardioversion under sedation/GA IV amiodarone added if DC shock unsuccessful
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Prolonged QT interval
* > 440 milliseconds in men* > 460 milliseconds in women
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Torsades de pointes
Polymorphic ventricular tachycardia
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Prolonged QT causes
- Long QT syndrome (inherited)- Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide)- Electrolyte disturbance
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Treatment for prolonged QT interval
B Blocker (not sotalol)Pacemaker or implacntable cardioverter
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Acute Mx of torsades de pointes
- Magnesium infusion - Defibrillation if ventricular tachycardia present
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Ventricular ectopics
Premature ventricular beats
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bigeminy
Every other beat is a ventricular ectopic (normal beat on ECG followed by ectopic beat) – b blockers might be used to manage symptoms
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First-degree heart block
PR >0.2 seconds (5 small or 1 big square)
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Second-degree heart block
When at instances P waves don’t follow QRS (some impulses don’t reach atrioventricular node and ventricles)
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Mobitz type 1 / Wenckebach phenomenon
Longer longer longer drop – increasing PR interval until P wave is not followed by QRS (2nd degree heart block)
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Mobitz type 2
Intermittent failure of conduction though av node – not all P waves are followed by QRS – ex ratio 3:1 or 2:1. PR interval remains normal
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Third-degree heart block
Complete heart block; no relation between P waves and QRS complex (risk of asystole)
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Bradycardia 3 main causes
Medications Heart blockSick sinus syndrome
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Sick sinus syndrome
dysfunction of the sinoatrial node (idiopathic degenerative fibrosis)
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Risk factors for asystole
* Mobitz type 2* Third-degree heart block (complete heart block)* Previous asystole* Ventricular pauses longer than 3 seconds
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atropine
Antimuscarinic, inhibits parasympathetic nervous system – leads to pupil dilation, dry mouth, urinary retention, constipation
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Temporary cardiac pacing
- Transcutaneous pacing- Transvenous pacing
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pacemaker
Consists of pulse generator and the pacing leads that carry electrical impulses to the parts of the heart. The wires are fed into the left subclavian vein and the chambers of the heart.
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Mx of unstable pts and at risk of asystole
* Intravenous atropine (first line)* Inotropes (e.g., isoprenaline or adrenaline)* Temporary cardiac pacing* Permanent implantable pacemaker, when available
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Which medical equipment is not compatible with the pacemakers
MRI scans, TENS machines, diathermy
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Indications for a pacemaker
* Symptomatic bradycardias (e.g., due to sick sinus syndrome)* Mobitz type 2 heart block* Third-degree heart block* Atrioventricular node ablation for atrial fibrillation* Severe heart failure (biventricular pacemakers)
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Biventricular / triple-chamber pacemaker
Have leads in right atrium, right ventricle, left ventricle Usually in patients with severe heart failure (cardiac resynchronisation therapy)
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Dual chamber pacemaker
Have leads in the right atrium and right ventricle
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Single chamber pacemaker
Has leads in a single chamber: right atrium or right ventricle
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Implantable cardioverter defibrillators
Continually monitor the heart and apply a defibrillator shock if they identify ventricular tachycardia or ventricular fibrillation
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Conditions requiring implantable cardioverter
* Previous cardiac arrest* Hypertrophic obstructive cardiomyopathy* Long QT syndrome
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Single chamber pacemaker on ECG
A line before either the P wave or QRS complex but not the other
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Dual chamber pacemaker on ECG
A line before both the P wave and QRS complex
